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THE SPRINGTIME PARTNERING EVENT
March 18–20, 2024 | Barcelona, SpainMarch 26–27, 2024 | Digital Partnering

CK Regeon Inc.

Profile

Founded in 2016, CK Regeon Inc. is developing First-in-class small molecule drugs which could restore damaged tissues of target diseases by restorative activation of the regenerative WNT/ꞵ-catenin signaling. The targeted diseases include obesity, diabetes, NASH, and Alzheimer's.Our platform technology is a regenerative therapy by safe activation of the WNT signaling which was suppressed in patient tissue cells by interfering function of CXXC5, a negative regulator of the WNT pathway.CXXC5 functions via binding at an upstream component, Dishevelled (Dvl), controlling the whole Wnt/ꞵ-catenin pathway involving regeneration of the damaged tissues of patients. The Wnt/ꞵ-catenin pathway is suppressed by cytosolic overexpression of CXXC5 in the patient tissue cells of the target diseases.The function control of CXXC5 by interfering its binding with Dvl results in therapeutic effects for the diseases suppressed Wnt/ꞵ-catenin signaling, including obese-diabetes, NASH, and Alzheimer's.Currently, our interest is obesity with diabetes. We confirm CXXC5 overexpression with the suppression of Wnt/ꞵ-catenin signaling in the tissue cells of both patient and animal models of the high fat diet (HFD) or db/db mutation. We confirmed the CXXC5-Dvl PPI as a target for developing obesity and diabetes drugs by pathophysiological analyses of Cxxc5-/- mice as well as by efficacy tests of the CXXC5-Dvl PPI inhibitor. CK Regeon develops small-molecule candidates revealing potent therapeutic effects by initial HTS of the compound library, followed by their evolution through long historical chemical synthesis and characterization. Our candidates reveal excellent therapeutic efficacies (20% weight loss in HFD-obesity model) without any significant side effects based on preclinical studies, including histochemical pathological analyses. These candidates could be developed as first-in-class, oral small-molecule drugs which potentially could replace GLP-1R agonist therapies.